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Clase terica 14

estructura de los virus

Preserial highresolution electron


microscope (1938)
from Siemens and
Halske. In 1939 first
EM micrograph of a
virus: TMV by
Ruska et al.

Bats are the reservoir host for viral pathogens, including Nipah,SARS, Ebola,
Hendra, Rabies.
MICROBE 2 (9): 418-419, 2007

Viruses in the sea


Curtis A. Suttle. Department of Chemistry, University of
California, Berkeley and the Molecular Foundry, Lawrence
Berkeley National Laboratory, Berkeley, California 94720, USA.
Viruses exist wherever life is found. They are a major cause of
mortality, a driver of global geochemical cycles and a reservoir
of the greatest genetic diversity on Earth. In the oceans, viruses
probably infect all living things, from bacteria to whales. They
affect the form of available nutrients and the termination of algal
blooms. Viruses can move between marine and terrestrial
reservoirs, raising the specter of emerging pathogens. Our
understanding of the effect of viruses on global systems and
processes continues to unfold, overthrowing the idea that viruses
and virus-mediated processes are sidebars to global processes.
Nature 437, 356-361 (15 September 2005)

PROPIEDADES DE LOS VIRUS USADAS PARA CONSTRUCCIONES TAXONOMICAS


A. PROPIEDADES DE LOS VIRIONES.
1. Tamao del virin
2. Forma del virin
3. Presencia o ausencia de envoltura y peplmeros
4. Simetra de los capsmeros y estructura.
B. PROPIEDADES DEL GENOMA
1. Tipo de cido nucleico - DNA o RNA
2. Cadena simple o doble.
3. Linear o Circular.
4. Cadena positiva o negativa
5. Nmero de segmentos.
6. Tamao del genoma.
C. PROPIEDADES DE LAS PROTEINAS
1. Nmero de las proteinas
2. Tamao de las proteinas.
3. Actividades funcionales de las proteinas(Especialmente
transcriptasa, transcriptasa reversa, hemaglutinina,
neuraminidasa y proteina de fusin)
D. SINTESIS DE MACROMOLECULAS
1. Estrategia de replicacin del cido nucleico.
2. Caractersticas de la transcripcin.
3. Caractersticas de la traduccin y procesamiento de
protenas
4. Lugar de acumulacin de las protenas virales, lugar de
ensamblaje, lugar de maduracin y liberacin.
5. Citopatologa, formacin de cuerpos de inclusin.
E. PROPIEDADES FISICAS
1. Estabilidad trmica y pH
2. Estabilidad en solventes, detergentes.
3. Estabilidad a la radiacin.
F. PROPIEDADES BIOLOGICAS
1. Serologa
2. Rango de huespedes.
3. Patogenicidad.
4. Tropismo tisular.
5. Transmisin y vectores.
6. Distribucin geogrfica.

ADENOVIRUS 80 nm D

PAPILLOMAVIRUS 55 nm D

HERPESVIRUS (100 nm D)

POLIOVIRUS (30 nm D)

INFLUENZA VIRUS (200 nm D)

Journal of Virology 74: 9646-9654, 2000

Journal of Virology 74: 9646-9654, 2000

PEPLOMEROS

FUNDAMENTAL VIROLOGY, FIELDS.

ESQUEMA PARCIAL DEL VIRUS INFLUENZA.


THE BIOLOGY OF ANIMAL VIRUSES, FENNER.

PEPLOMEROS

FUNDAMENTAL VIROLOGY, FIELDS

CICLO DE MULTIPLICACION

1. ADSORCION.

- ES ESPECIFICA (RECEPTORES EN LA SUPERFICIE DE LA CELULA).

2. PENETRACION.
- VARIA DE ACUERDO AL VIRUS

3. DECAPSIDACION.

Figure 1. Steps in the Endocytic Entry Program of a


Typical Animal Virus
Many viruses depend on the host cell's endocytic
pathways for entry. In this example, the virus
proceeds to deliver its uncoated genome into the
nucleoplasm. The interaction between the virus and
the host cell starts with virus binding to attachment
factors and receptors on the cell surface, followed
by lateral movement of the virus-receptor complexes
and the induction of signals that result in the
endocytic internalization of the virus particle. After
vesicular trafficking and delivery into the lumen of
endosomes, caveosomes, or the ER, a change in the
virus conformation is induced by cellular cues. This
alteration results in the penetration of the virus or its
capsids through the vacuole membrane into the
cytosolic compartment. Enveloped viruses use
membrane fusion for penetration, whereas
nonenveloped viruses induce lysis or pore
formation. After targeting and transport along
microtubules, the virus or the capsid binds, as in this
example, to the nuclear pore complex, undergoes a
final conversion, and releases the viral genome into
the nucleus. The details in the entry program vary
for different viruses and cell types, but many of the
key steps shown here are general.
CELL 124(4): 729-740, 2006

CELL 124(4): 729-740, 2006

Figure 2. Endocytic Pathways Used by Viruses


In mammalian cells, many different mechanisms are available for the endocytic
internalization of virus particles. Some of these mechanisms, such as clathrinmediated endocytosis, are ongoing, whereas others, such as caveolae, are ligand
and cargo induced. Currently, there is evidence for six pathways.
(A) Macropinocytosis is involved in the entry of adenoviruses.
(B) A clathrin-independent pathway from the plasma membrane has been shown to
exist for influenza virus and arenaviruses.
(C) The clathrin-mediated pathway is the most commonly observed uptake
pathway for viruses. The viruses are transported via early endosomes to late
endosomes and eventually to lysosomes.
(D) The caveolar pathway is one of several closely related, cholesterol-dependent
pathways that bring viruses including SV40, coxsackie B, mouse polyoma, and
Echo 1 to caveosomes, from which many of them continue, by a second vesicle
transport step, to the ER.
(E) A cholesterol-dependent endocytic pathway devoid of clathrin and caveolin-1,
used by polyomavirus and SV40.
(F) A pathway similar to (D) except dependent on dynamin-2. It is used by Echo
virus 1.
CELL 124(4): 729-740, 2006

PRIMEROS ESTADIOS DE INFECCION POR SEMLINKI FORESSST VIRUS,


MICROBIOLOGY, DAVIS.

CELL 124(4): 729-740, 2006

Figure 3. Electron Micrographs Showing Virus Internalization by Clathrin- or


Caveolar/Raft-Mediated Endocytosis
(A and B) Semliki Forest virus, a 70 nm diameter enveloped alphavirus, is
internalized by clathrin-coated pits (A) and vesicles (B) for endocytosis and
infection. Here, the virus is interacting with a BHK-21 cell.
(C and D) Simian virus 40, a small 50 nm diameter nonenveloped DNA virus, binds
to gangliosides in the plasma membrane of CV-1 cells and enters via caveolae (C)
and tight-fitting small vesicles. The viruses are transported through caveosomes to
the ER, where many accumulate in smooth membrane domains (D).
Scale bar in (A) and (C) = 100 nm, (B) = 200 nm, and (D) = 250 nm.

CLATRINA-VACUOLAS

JOURNAL OF VIROLOGY 74:1342-1354, 2000

MECANISMO PROBABLE DE TRANSFERENCIA DEL RNA DEL


POLIOVIRUS A TRAVES DE LA MEMBRANA CELULAR (PROTEINAS
VIRALES: VP1 ; VP2 ; VP3 ; VP4).
Journal of Virology 74: 1342-1354, 2000

Figure 1. Incoming Adenovirus


Type 2 Particles Are Associated
with Microtubules
Single 120 nm optical section
from a confocal laser scanning
microscope showing the
microtubule cytoskeleton
(green) of a HeLa cell infected
with Texas red-labeled Ad2
particles (red) for 30 min.
Enlarged insets highlight the
colocalization of Ad2 particles
(arrowheads) with microtubules
in the periphery of the cell.
Bars, 10 m and 2 m (inset),
respectively.

CELL 124(4): 741-754, 2006

CICLO DE MULTIPLICACION

3. SINTESIS DE MACROMOLECULAS VIRALES

- TRANSCRIPCION:
mRNA TEMPRANO: SINTESIS DE PROTEINAS PARA REPLICACION
mRNA TARDIO:

SINTESIS DE PROTEINAS ESTRUCTURALES.

- TRADUCCION

- REPLICACION

4. ENSAMBLAJE Y LIBERACION

MICROBIOLOGY, DAVIS.

MULTIPLICACION DE UN RETROVIRUS

Cell 138: 31-50, 2009

Figure 1. The Course of Viral Infection

Figure 1. The Course of Viral Infection


When a virus enters the host, there is an initial nonequilibrium
phase of acute infection. During this phase, viral and immune
strategies compete for dominance.
Assuming the host survives, a decision point is reached at which
the infection is either cleared or becomes chronic. This decision
point may be reached very early in infection for viruses that can
establish a latent infection, in which case the infection is
permanent regardless of the course of acute infection.
If recovery occurs, the immune system must reset by clearing the
antigen and re-establishing immune homeostasis. If the balance
shifts toward chronic infection, a new set of viral and host
strategies interact to define a metastable equilibrium in which
viral replication is held in check, but the virus is not cleared.

Figure 2. Chronic Viral Infections in Humans

Cell 138: 31-50, 2009

Figure 2. Chronic Viral Infections in Humans


The number of humans infected with different chronic viruses is
estimated from the percentage of humans carrying a given virus,
(estimated by the prevalence of antiviral antibodies in serum)
and assuming that the world population is 6.75 billion.
For adenovirus, the situation is unclear and the prevalence of
chronic infection is arbitrarily set at 1%. For some viruses, the
prevalence of infection is not sufficiently well defined for
inclusion in the graph. These include xenotropic murine
leukemia virus-related virus (XMLV), human T cell leukemia
virus (HTLV II, III, IV), and polyomaviruses MC, KI, and WU.
The estimates in the graph are approximate as they apply data
on prevalence in the limited populations studied to date to the
global human population.